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564 results on '"Strong, Louise"'

1. Bayesian estimation of a semiparametric recurrent event model with applications to the penetrance estimation of multiple primary cancers in Li-Fraumeni Syndrome

Author

Shin, Seung Jun, Li, Jialu, Ning, Jing, Bojadzieva, Jasmina, Strong, Louise C., and Wang, Wenyi

Subjects
Statistics - Applications
Abstract

A common phenomenon in cancer syndromes is for an individual to have multiple primary cancers at different sites during his/her lifetime. Patients with Li-Fraumeni syndrome (LFS), a rare pediatric cancer syndrome mainly caused by germline TP53 mutations, are known to have a higher probability of developing a second primary cancer than those with other cancer syndromes. In this context, it is desirable to model the development of multiple primary cancers to enable better clinical management of LFS. Here, we propose a Bayesian recurrent event model based on a non-homogeneous Poisson process in order to obtain penetrance estimates for multiple primary cancers related to LFS. We employed a family-wise likelihood that facilitates using genetic information inherited through the family pedigree and properly adjusted for the ascertainment bias that was inevitable in studies of rare diseases by using an inverse probability weighting scheme. We applied the proposed method to data on LFS, using a family cohort collected through pediatric sarcoma patients at MD Anderson Cancer Center from 1944 to 1982. Both internal and external validation studies showed that the proposed model provides reliable penetrance estimates for multiple primary cancers in LFS, which, to the best of our knowledge, have not been reported in the LFS literature.

Published
2018

2. Bayesian Semiparametric Estimation of Cancer-specific Age-at-onset Penetrance with Application to Li-Fraumeni Syndrome

Author

Shin, Seung Jun, Yuan, Ying, Strong, Louise C., Bojadzieva, Jasmina, and Wang, Wenyi

Subjects
Statistics - Applications
Abstract

Penetrance, which plays a key role in genetic research, is defined as the proportion of individuals with the genetic variants (i.e., {genotype}) that cause a particular trait and who have clinical symptoms of the trait (i.e., {phenotype}). We propose a Bayesian semiparametric approach to estimate the cancer-specific age-at-onset penetrance in the presence of the competing risk of multiple cancers. We employ a Bayesian semiparametric competing risk model to model the duration until individuals in a high-risk group develop different cancers, and accommodate family data using family-wise likelihoods. We tackle the ascertainment bias arising when family data are collected through probands in a high-risk population in which disease cases are more likely to be observed. We apply the proposed method to a cohort of 186 families with Li-Fraumeni syndrome identified through probands with sarcoma treated at MD Anderson Cancer Center from 1944 to 1982.

Published
2017

3. Long‐term sequelae in survivors of childhood leukemia with Down syndrome: A childhood cancer survivor study report

Author

Goldsby, Robert E, Stratton, Kayla L, Raber, Shannon, Ablin, Arthur, Strong, Louise C, Oeffinger, Kevin, Sklar, Charles A, Armstrong, Gregory T, Robison, Leslie L, Bhatia, Smita, and Leisenring, Wendy M

Subjects
Pediatric, Rare Diseases, Rehabilitation, Intellectual and Developmental Disabilities (IDD), Pediatric Research Initiative, Hematology, Prevention, Brain Disorders, Pediatric Cancer, Cancer, Clinical Research, Childhood Leukemia, Down Syndrome, 2.1 Biological and endogenous factors, Aetiology, Adolescent, Adult, Cancer Survivors, Child, Chronic Disease, Female, Humans, Leukemia, Male, Middle Aged, Neoplasms, Second Primary, Proportional Hazards Models, Young Adult, Down syndrome, leukemia, late effects, chronic conditions, survivorship, Oncology and Carcinogenesis, Public Health and Health Services, Oncology & Carcinogenesis
Abstract

BackgroundChildren with Down syndrome (DS) are at increased risk of developing acute leukemia and are more prone to acute toxicities. We studied the incidence and severity of chronic health conditions among survivors of childhood leukemia with DS compared with those without DS.MethodsChronic health conditions reported by questionnaire were compared between 154 pediatric leukemia survivors with DS and 581 without DS, matched by leukemia, age at diagnosis, race/ethnicity, sex, radiation location and chemotherapy exposure using Cox models to estimate hazard ratios (HRs) and 95% confidence intervals (CIs). Subjects were selected from 7139 5-year survivors of leukemia in the Childhood Cancer Survivor Study.ResultsRisk of at least 1 late onset chronic health condition (grade 1-5) was similar in the DS population compared with the non-DS group (HR, 1.1; 95% CI, 0.7-1.5). Serious chronic health conditions (grade 3-5) were more common in DS survivors (HR, 1.7; 95% CI, 1.1-2.6), as were ≥ 3 chronic health conditions (grades 1-5) (HR, 1.7; 95% CI, 1.2-2.4). The 25-year cumulative incidence of any condition (grades 1-5) was 83% for DS survivors and 69% for non-DS survivors.ConclusionLeukemia survivors with DS have therapy-related chronic health conditions comparable to those of similarly treated survivors without DS, with a few notable exceptions: 1) an increased risk of cataracts, hearing loss, and thyroid dysfunction compared with survivors without DS (though these are known risks in the DS population), 2) decreased risk of second cancers, and 3) increased risk of severe or multiple conditions. Practitioners should be aware of these risks during and after therapy. Cancer 2018;124:617-25. © 2017 American Cancer Society.

Published
2018

4. Genetic susceptibility to radiation-induced breast cancer after Hodgkin lymphoma

Author

Opstal-van Winden, Annemieke W.J., de Haan, Hugoline G., Hauptmann, Michael, Schmidt, Marjanka K., Broeks, Annegien, Russell, Nicola S., Janus, Cécile P.M., Krol, Augustinus D.G., van der Baan, Frederieke H., De Bruin, Marie L., van Eggermond, Anna M., Dennis, Joe, Anton-Culver, Hoda, Haiman, Christopher A., Sawyer, Elinor J., Cox, Angela, Devilee, Peter, Hooning, Maartje J., Peto, Julian, Couch, Fergus J., Pharoah, Paul, Orr, Nick, Easton, Douglas F., Aleman, Berthe M.P., Strong, Louise C., Bhatia, Smita, Cooke, Rosie, Robison, Leslie L., Swerdlow, Anthony J., and van Leeuwen, Flora E.

Published
2019
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5. Long-term risk of medical conditions associated with breast cancer treatment

Author

Hill, Deirdre A, Horick, Nora K, Isaacs, Claudine, Domchek, Susan M, Tomlinson, Gail E, Lowery, Jan T, Kinney, Anita Y, Berg, Jonathan S, Edwards, Karen L, Moorman, Patricia G, Plon, Sharon E, Strong, Louise C, Ziogas, Argyrois, Griffin, Constance A, Kasten, Carol H, and Finkelstein, Dianne M

Subjects
Osteoporosis, Clinical Research, Prevention, Breast Cancer, Aging, Rehabilitation, Cancer, Cardiovascular, Heart Disease, Heart Disease - Coronary Heart Disease, Detection, screening and diagnosis, 4.2 Evaluation of markers and technologies, Adult, Aged, Antineoplastic Agents, Bone Diseases, Metabolic, Breast Neoplasms, Female, Heart Diseases, Humans, Lymph Node Excision, Lymphedema, Middle Aged, Prevalence, Radiotherapy, Risk Factors, Surveys and Questionnaires, Survivors, Breast neoplasms, Heart disease, Chemotherapy, Clinical Sciences, Oncology and Carcinogenesis, Oncology & Carcinogenesis
Abstract

Early and late effects of cancer treatment are of increasing concern with growing survivor populations, but relevant data are sparse. We sought to determine the prevalence and hazard ratio of such effects in breast cancer cases. Women with invasive breast cancer and women with no cancer history recruited for a cancer research cohort completed a mailed questionnaire at a median of 10 years post-diagnosis or matched reference year (for the women without cancer). Reported medical conditions including lymphedema, osteopenia, osteoporosis, and heart disease (congestive heart failure, myocardial infarction, coronary heart disease) were assessed in relation to breast cancer therapy and time since diagnosis using Cox regression. The proportion of women currently receiving treatment for these conditions was calculated. Study participants included 2,535 women with breast cancer and 2,428 women without cancer (response rates 66.0 % and 50.4 %, respectively) Women with breast cancer had an increased risk of lymphedema (Hazard ratio (HR) 8.6; 95 % confidence interval (CI) 6.3-11.6), osteopenia (HR 2.1; 95 % CI 1.8-2.4), and osteoporosis (HR 1.5; 95 % CI 1.2-1.9) but not heart disease, compared to women without cancer Hazard ratios varied by treatment and time since diagnosis. Overall, 49.3 % of breast cancer cases reported at least one medical condition, and at 10 or more years post-diagnosis, 37.7 % were currently receiving condition-related treatment. Responses from survivors a decade following cancer diagnosis demonstrate substantial treatment-related morbidity, and emphasize the need for continued medical surveillance and follow-up care into the second decade post-diagnosis.

Published
2014

6. Understanding the role of the business community in the making of UK climate policy between 1997 and 2009

Author

Strong, Louise

Subjects
363.73874
Abstract

Business activity is directly responsible for around fifty percent of UK emissions and academics and NGOs have often referred to the influence of corporate actors when trying to explain the UK government's failure to reduce emissions. Yet, surprisingly little academic research has sought to unpack the nature of the business community's role in policymaking or understand the processes and mechanisms by which business actors are able to shape climate policy. Drawing on interviews with 55 business elites, British policymakers and other key stakeholders, this thesis seeks to address these questions by providing a detailed analysis of the business community's role in the making of UK climate policy. In particular, it examines the degree of involvement which the business community has had in the policymaking process, and considers whether, and if so why, corporate actors have enjoyed a privileged position. It uses the concept of strategic selectivity and insights from work on environmental discourse to help make sense of the advantages and constraints faced by companies and business groups. Case study chapters explore the role of the CBI in climate policymaking, business actors' influence on the development of emissions trading, and Large Electricity Producers' impact on policy to decarbonise generation. While recognising that 'the business community' requires considerable disaggregation when it comes to climate change, and that cleavages between firms and sectors limit corporate influence, this thesis suggests that there is analytical purchase to the concept of a business community. Firstly, business actors have together been constrained by aspects of the prevailing UK context. Most notably, the environmental movement and sections of the media have played a crucial role in shaping the political agenda and delegitimising a reactionary corporate approach to climate change. Cross-party competition has further restricted business actors' room for manoeuvre on the issue. Secondly, companies and business groups have enjoyed similar advantages when it comes to climate policy: corporate interests have together benefited from several discursive aspects of the strategically selective setting in the UK. In particular, policymakers' preference for market-based policy solutions and their privileging of economic growth. A widespread attachment in British society to high levels of consumption and personal travel has also facilitated corporate interests politically. Business actors have also been advantaged during policymaking because they have generally been rich in material resources - information, 10 technical expertise and capital - highly valued by government. Policymakers have felt that they rely on business actors for information to make feasible and effective policy. Likewise, in order to achieve its twin objectives of emissions reductions and low carbon growth, the government has looked to companies for their ability to innovate and invest. The political dominance in the UK of a discourse of ecological modernisation has made the capacity to innovate and invest particularly important to government, and has also helped legitimise and safeguard the core objective which corporate actors share - continued business growth. This study has found that business groups and leaders have facilitated their political influence by pushing this positive win-win discourse and by adopting a constructive approach to climate policy.

Published
2011

7. Activating mutation in MET oncogene in familial colorectal cancer

Author

Neklason, Deborah W, Done, Michelle W, Sargent, Nykole R, Schwartz, Ann G, Anton-Culver, Hoda, Griffin, Constance A, Ahnen, Dennis J, Schildkraut, Joellen M, Tomlinson, Gail E, Strong, Louise C, Miller, Alexander R, Stopfer, Jill E, and Burt, Randall W

Abstract

Abstract Background In developed countries, the lifetime risk of developing colorectal cancer (CRC) is 5%, and it is the second leading cause of death from cancer. The presence of family history is a well established risk factor with 25-35% of CRCs attributable to inherited and/or familial factors. The highly penetrant inherited colon cancer syndromes account for approximately 5%, leaving greater than 20% without clear genetic definition. Familial colorectal cancer has been linked to chromosome 7q31 by multiple affected relative pair studies. The MET proto-oncogene which resides in this chromosomal region is considered a candidate for genetic susceptibility. Methods MET exons were amplified by PCR from germline DNA of 148 affected sibling pairs with colorectal cancer. Amplicons with altered sequence were detected with high-resolution melt-curve analysis using a LightScanner (Idaho Technologies). Samples demonstrating alternative melt curves were sequenced. A TaqMan assay for the specific c.2975C > T change was used to confirm this mutation in a cohort of 299 colorectal cancer cases and to look for allelic amplification in tumors. Results Here we report a germline non-synonymous change in the MET proto-oncogene at amino acid position T992I (also reported as MET p.T1010I) in 5.2% of a cohort of sibling pairs affected with CRC. This genetic variant was then confirmed in a second cohort of individuals diagnosed with CRC and having a first degree relative with CRC at prevalence of 4.1%. This mutation has been reported in cancer cells of multiple origins, including 2.5% of colon cancers, and in

Published
2011

10. Analysis of Co-Aggregation of Cancer Based on Registry Data

Author

Matthews, Abigail G, Betensky, Rebecca A, Anton-Culver, Hoda, Bowen, Deborah, Griffin, Constance, Isaacs, Claudine, Kasten, Carol, Mineau, Geraldine, Nayfield, Susan, Schildkraut, Joellen, Strong, Louise, Weber, Barbara, and Finkelstein, Dianne M

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Ovarian Cancer, Colo-Rectal Cancer, Rare Diseases, Cancer, Digestive Diseases, Clinical Research, Pancreatic Cancer, 2.1 Biological and endogenous factors, Aetiology, Female, Humans, Male, Neoplasms, Registries, familial aggregation, association, family study, Cancer Genetics Network, Medical Biotechnology, Clinical Sciences, Public Health and Health Services, Genetics & Heredity, Clinical sciences, Public health
Abstract

ObjectiveAn exploratory analysis of co-aggregation of cancers using registry-based data.MethodsWe utilized sibships from over 18,000 families who had been recruited to the NCI-sponsored multi-institutional Cancer Genetics Network. The analysis assesses co-aggregation at the individual and family level and adjusts for ascertainment.ResultsWe found statistically significant familial co-aggregation of lung cancer with pancreatic (adjusted p < 0.001), prostate (adjusted p < 0.003), and colorectal cancers (adjusted p = 0.004). In addition, we found significant familial co-aggregation of pancreatic and colorectal cancers (adjusted p = 0.018), and co-aggregation of hematopoietic and (non-ovarian) gynecologic cancers (adjusted p = 0.01).ConclusionThis analysis identified familial aggregation of cancers for which a genetic component has yet to be established.

Published
2006

11. The Cancer Genetics Network: Recruitment Results and Pilot Studies

Author

Anton-Culver, Hoda, Ziogas, Argyrios, Bowen, Deborah, Finkelstein, Dianne, Griffin, Constance, Hanson, James, Isaacs, Claudine, Kasten-Sportes, Carol, Mineau, Geraldine, Nadkarni, Prakash, Rimer, Barbara, Schildkraut, Joellen, Strong, Louise, Weber, Barbara, Winn, Deborah, Hiatt, Robert, and Nayfield, Susan

Subjects
Health Services and Systems, Biomedical and Clinical Sciences, Health Sciences, Oncology and Carcinogenesis, Genetics, Cancer, Human Genome, Genetic Testing, 2.1 Biological and endogenous factors, Aetiology, Good Health and Well Being, Female, Genetic Services, Government Programs, Humans, Male, National Institutes of Health (U.S.), Neoplasms, Pilot Projects, United States, National Institutes of Health, Medical Biotechnology, Clinical Sciences, Public Health and Health Services, Genetics & Heredity, Clinical sciences, Public health
Abstract

ObjectiveThe National Cancer Institute established the Cancer Genetics Network (CGN) to support collaborative investigations into the genetic basis of cancer susceptibility, explore mechanisms to integrate this new knowledge into medical practice, and identify ways of addressing the associated psychosocial, ethical, legal, and public health issues.Subjects and methodsThe CGN has developed the complex infrastructure required to support the projects, including the establishment of guidelines and policies, uniform methods, standard questionnaires to be used by all of the centers, and a standard format for submission of data to the Informatics Center. Cancer patients and their family members have been invited to enroll and be included in a pool of potential study participants. The Information Technology Group is responsible for support of the design, implementation, and maintenance of the multicenter Network-wide research protocols.ResultsAs of January 2004, the CGN contained data on 23,995 probands (participants) and 425,798 family members. As a resource for cancer genetic studies, the CGN has a large number of probands and first-degree relatives with and without cancer and with multiple ethnicities. Different study designs can be used including case-control, case-case, and family studies.ConclusionsThe unique resources of the CGN are available for studies on cancer genetic susceptibility, translational research, and behavioral research. The CGN is now at a point where approved collaborators may have access to enrolled patients and their families for special studies, as well as to the clinical, environmental and family cancer history data banked in the Informatics Center.

Published
2003

14. Supplementary figures from Recommended Guidelines for Validation, Quality Control, and Reporting of TP53 Variants in Clinical Practice

Author

Leroy, Bernard, primary, Ballinger, Mandy L., primary, Baran-Marszak, Fanny, primary, Bond, Gareth L., primary, Braithwaite, Antony, primary, Concin, Nicole, primary, Donehower, Lawrence A., primary, El-Deiry, Wafik S., primary, Fenaux, Pierre, primary, Gaidano, Gianluca, primary, Langerød, Anita, primary, Hellstrom-Lindberg, Eva, primary, Iggo, Richard, primary, Lehmann-Che, Jacqueline, primary, Mai, Phuong L., primary, Malkin, David, primary, Moll, Ute M., primary, Myers, Jeffrey N., primary, Nichols, Kim E., primary, Pospisilova, Sarka, primary, Ashton-Prolla, Patricia, primary, Rossi, Davide, primary, Savage, Sharon A., primary, Strong, Louise C., primary, Tonin, Patricia N., primary, Zeillinger, Robert, primary, Zenz, Thorsten, primary, Fraumeni, Joseph F., primary, Taschner, Peter E.M., primary, Hainaut, Pierre, primary, and Soussi, Thierry, primary

Published
2023
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17. Data from Recommended Guidelines for Validation, Quality Control, and Reporting of TP53 Variants in Clinical Practice

Author

Leroy, Bernard, primary, Ballinger, Mandy L., primary, Baran-Marszak, Fanny, primary, Bond, Gareth L., primary, Braithwaite, Antony, primary, Concin, Nicole, primary, Donehower, Lawrence A., primary, El-Deiry, Wafik S., primary, Fenaux, Pierre, primary, Gaidano, Gianluca, primary, Langerød, Anita, primary, Hellstrom-Lindberg, Eva, primary, Iggo, Richard, primary, Lehmann-Che, Jacqueline, primary, Mai, Phuong L., primary, Malkin, David, primary, Moll, Ute M., primary, Myers, Jeffrey N., primary, Nichols, Kim E., primary, Pospisilova, Sarka, primary, Ashton-Prolla, Patricia, primary, Rossi, Davide, primary, Savage, Sharon A., primary, Strong, Louise C., primary, Tonin, Patricia N., primary, Zeillinger, Robert, primary, Zenz, Thorsten, primary, Fraumeni, Joseph F., primary, Taschner, Peter E.M., primary, Hainaut, Pierre, primary, and Soussi, Thierry, primary

Published
2023
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22. Supplementary Figure 4 from Common Familial Colorectal Cancer Linked to Chromosome 7q31: A Genome-Wide Analysis

Author

Neklason, Deborah W., primary, Kerber, Richard A., primary, Nilson, David B., primary, Anton-Culver, Hoda, primary, Schwartz, Ann G., primary, Griffin, Constance A., primary, Lowery, Jan T., primary, Schildkraut, Joellen M., primary, Evans, James P., primary, Tomlinson, Gail E., primary, Strong, Louise C., primary, Miller, Alexander R., primary, Stopfer, Jill E., primary, Finkelstein, Dianne M., primary, Nadkarni, Prakash M., primary, Kasten, Carol H., primary, Mineau, Geraldine P., primary, and Burt, Randall W., primary

Published
2023
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23. Supplementary Figure 1 from Common Familial Colorectal Cancer Linked to Chromosome 7q31: A Genome-Wide Analysis

Author

Neklason, Deborah W., primary, Kerber, Richard A., primary, Nilson, David B., primary, Anton-Culver, Hoda, primary, Schwartz, Ann G., primary, Griffin, Constance A., primary, Lowery, Jan T., primary, Schildkraut, Joellen M., primary, Evans, James P., primary, Tomlinson, Gail E., primary, Strong, Louise C., primary, Miller, Alexander R., primary, Stopfer, Jill E., primary, Finkelstein, Dianne M., primary, Nadkarni, Prakash M., primary, Kasten, Carol H., primary, Mineau, Geraldine P., primary, and Burt, Randall W., primary

Published
2023
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24. Supplementary Figure 2 from Common Familial Colorectal Cancer Linked to Chromosome 7q31: A Genome-Wide Analysis

Author

Neklason, Deborah W., primary, Kerber, Richard A., primary, Nilson, David B., primary, Anton-Culver, Hoda, primary, Schwartz, Ann G., primary, Griffin, Constance A., primary, Lowery, Jan T., primary, Schildkraut, Joellen M., primary, Evans, James P., primary, Tomlinson, Gail E., primary, Strong, Louise C., primary, Miller, Alexander R., primary, Stopfer, Jill E., primary, Finkelstein, Dianne M., primary, Nadkarni, Prakash M., primary, Kasten, Carol H., primary, Mineau, Geraldine P., primary, and Burt, Randall W., primary

Published
2023
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25. Data from Common Familial Colorectal Cancer Linked to Chromosome 7q31: A Genome-Wide Analysis

Author

Neklason, Deborah W., primary, Kerber, Richard A., primary, Nilson, David B., primary, Anton-Culver, Hoda, primary, Schwartz, Ann G., primary, Griffin, Constance A., primary, Lowery, Jan T., primary, Schildkraut, Joellen M., primary, Evans, James P., primary, Tomlinson, Gail E., primary, Strong, Louise C., primary, Miller, Alexander R., primary, Stopfer, Jill E., primary, Finkelstein, Dianne M., primary, Nadkarni, Prakash M., primary, Kasten, Carol H., primary, Mineau, Geraldine P., primary, and Burt, Randall W., primary

Published
2023
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26. Supplementary Figure 3 from Common Familial Colorectal Cancer Linked to Chromosome 7q31: A Genome-Wide Analysis

Author

Neklason, Deborah W., primary, Kerber, Richard A., primary, Nilson, David B., primary, Anton-Culver, Hoda, primary, Schwartz, Ann G., primary, Griffin, Constance A., primary, Lowery, Jan T., primary, Schildkraut, Joellen M., primary, Evans, James P., primary, Tomlinson, Gail E., primary, Strong, Louise C., primary, Miller, Alexander R., primary, Stopfer, Jill E., primary, Finkelstein, Dianne M., primary, Nadkarni, Prakash M., primary, Kasten, Carol H., primary, Mineau, Geraldine P., primary, and Burt, Randall W., primary

Published
2023
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27. Supplementary Figure Legends 1-4 from Common Familial Colorectal Cancer Linked to Chromosome 7q31: A Genome-Wide Analysis

Author

Neklason, Deborah W., primary, Kerber, Richard A., primary, Nilson, David B., primary, Anton-Culver, Hoda, primary, Schwartz, Ann G., primary, Griffin, Constance A., primary, Lowery, Jan T., primary, Schildkraut, Joellen M., primary, Evans, James P., primary, Tomlinson, Gail E., primary, Strong, Louise C., primary, Miller, Alexander R., primary, Stopfer, Jill E., primary, Finkelstein, Dianne M., primary, Nadkarni, Prakash M., primary, Kasten, Carol H., primary, Mineau, Geraldine P., primary, and Burt, Randall W., primary

Published
2023
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30. Genome-Wide Association Study to Identify Susceptibility Loci That Modify Radiation-Related Risk for Breast Cancer After Childhood Cancer

Author

Morton, Lindsay M., Sampson, Joshua N., Armstrong, Gregory T., Chen, Ting-Huei, Hudson, Melissa M., Karlins, Eric, Dagnall, Casey L., Li, Shengchao Alfred, Wilson, Carmen L., Srivastava, Deo Kumar, Liu, Wei, Kang, Guolian, Oeffinger, Kevin C., Henderson, Tara O., Moskowitz, Chaya S., Gibson, Todd M., Merino, Diana M., Wong, Jeannette R., Hammond, Sue, Neglia, Joseph P., Turcotte, Lucie M., Miller, Jeremy, Bowen, Laura, Wheeler, William A., Leisenring, Wendy M., Whitton, John A., Burdette, Laurie, Chung, Charles, Hicks, Belynda D., Jones, Kristine, Machiela, Mitchell J., Vogt, Aurelie, Wang, Zhaoming, Yeager, Meredith, Neale, Geoffrey, Lear, Matthew, Strong, Louise C., Yasui, Yutaka, Stovall, Marilyn, Weathers, Rita E., Smith, Susan A., Howell, Rebecca, Davies, Stella M., Radloff, Gretchen A., Onel, Kenan, de González, Amy Berrington, Inskip, Peter D., Rajaraman, Preetha, Fraumeni, Joseph F., Jr., Bhatia, Smita, Chanock, Stephen J., Tucker, Margaret A., and Robison, Leslie L.

Published
2017
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31. Baseline Surveillance in Li-Fraumeni Syndrome Using Whole-Body Magnetic Resonance Imaging: A Meta-analysis

Author

Ballinger, Mandy L., Best, Ana, Mai, Phuong L., Khincha, Payal P., Loud, Jennifer T., Peters, June A., Achatz, Maria Isabel, Chojniak, Rubens, Balieiro da Costa, Alexandre, Santiago, Karina Miranda, Garber, Judy, O’Neill, Allison F., Eeles, Rosalind A., Evans, D. Gareth, Bleiker, Eveline, Sonke, Gabe S., Ruijs, Marielle, Loo, Claudette, Schiffman, Joshua, Naumer, Anne, Kohlmann, Wendy, Strong, Louise C., Bojadzieva, Jasmina, Malkin, David, Rednam, Surya P., Stoffel, Elena M., Koeppe, Erika, Weitzel, Jeffrey N., Slavin, Thomas P., Nehoray, Bita, Robson, Mark, Walsh, Michael, Manelli, Lorenzo, Villani, Anita, Thomas, David M., and Savage, Sharon A.

Published
2017
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32. Li-Fraumeni syndrome: report of a clinical research workshop and creation of a research consortium

Author

Mai, Phuong L., Malkin, David, Garber, Judy E., Schiffman, Joshua D., Weitzel, Jeffrey N., Strong, Louise C., Wyss, Oliver, Locke, Luana, Means, Von, Achatz, Maria Isabel, Hainaut, Pierre, Frebourg, Thierry, Evans, D. Gareth, Bleiker, Eveline, Patenaude, Andrea, Schneider, Katherine, Wilfond, Benjamin, Peters, June A., Hwang, Paul M., Ford, James, Tabori, Uri, Ognjanovic, Simona, Dennis, Phillip A., Wentzensen, Ingrid M., Greene, Mark H., Fraumeni, Joseph F., Jr., and Savage, Sharon A.

Published
2012
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33. A genome-wide meta-analysis of nodular sclerosing Hodgkin lymphoma identifies risk loci at 6p21.32

Author

Cozen, Wendy, Li, Dalin, Best, Timothy, Van Den Berg, David J., Gourraud, Pierre-Antoine, Cortessis, Victoria K., Skol, Andrew D., Mack, Thomas M., Glaser, Sally L., Weiss, Lawrence M., Nathwani, Bharat N., Bhatia, Smita, Schumacher, Fredrick R., Edlund, Christopher K., Hwang, Amie E., Slager, Susan L., Fredericksen, Zachary S., Strong, Louise C., Habermann, Thomas M., Link, Brian K., Cerhan, James R., Robison, Leslie L., Conti, David V., and Onel, Kenan

Published
2012
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34. Analysis of Co-Aggregation of Cancer Based on Registry Data

Author

Matthews, Abigail G., Betensky, Rebecca A., Anton-Culver, Hoda, Bowen, Deborah, Griffin, Constance, Isaacs, Claudine, Kasten, Carol, Mineau, Geraldine, Nayfield, Susan, Schildkraut, Joellen, Strong, Louise, Weber, Barbara, and Finkelstein, Dianne M.

Published
2006

35. In Support of a Patient-Driven Initiative and Petition to Lower the High Price of Cancer Drugs

Author

Tefferi, Ayalew, Kantarjian, Hagop, Rajkumar, Vincent S., Baker, Lawrence H., Abkowitz, Jan L., Adamson, John W., Hira Advani, Ranjana, Allison, James, Antman, Karen H., Bast, Robert C., Jr., Bennett, John M., Benz, Edward J., Jr., Berliner, Nancy, Bertino, Joseph, Bhatia, Ravi, Bhatia, Smita, Bhojwani, Deepa, Blanke, Charles D., Bloomfield, Clara D., Bosserman, Linda, Broxmeyer, Hal E., Byrd, John C., Cabanillas, Fernando, Peter Canellos, George, Chabner, Bruce A., Chanan-Khan, Asher, Cheson, Bruce, Clarkson, Bayard, Cohn, Susan L., Colon-Otero, Gerardo, Cortes, Jorge, Coutre, Steven, Cristofanilli, Massimo, Curran, Walter J., Jr., Daley, George Q., DeAngelo, Daniel J., Deeg, Joachim H., Einhorn, Lawrence H., Erba, Harry P., Esteva, Francisco J., Estey, Elihu, Fidler, Isaiah J., Foran, James, Forman, Stephen, Freireich, Emil, Fuchs, Charles, George, James N., Gertz, Morie A., Giralt, Sergio, Golomb, Harvey, Greenberg, Peter, Gutterman, Jordan, Handin, Robert I., Hellman, Samuel, Marcelo Hoff, Paulo, Hoffman, Ronald, Ki Hong, Waun, Horowitz, Mary, Hortobagyi, Gabriel N., Hudis, Clifford, Pierre Issa, Jean, Evan Johnson, Bruce, Kantoff, Philip W., Kaushansky, Kenneth, Khayat, David, Khuri, Fadlo R., Kipps, Thomas J., Kripke, Margaret, Kyle, Robert A., Larson, Richard A., Lawrence, Theodore S., Levine, Ross, Link, Michael P., Lippman, Scott M., Lonial, Sagar, Lyman, Gary H., Markman, Maurie, Mendelsohn, John, Meropol, Neal J., Messinger, Yoav, Mulvey, Therese M., OʼBrien, Susan, Perez-Soler, Roman, Pollock, Raphael, Prchal, Josef, Press, Oliver, Radich, Jerald, Rai, Kanti, Rosenberg, Saul A., Rowe, Jacob M., Rugo, Hope, Runowicz, Carolyn D., Sandmaier, Brenda M., Saven, Alan, Schafer, Andrew I., Schiffer, Charles, Sekeres, Mikkael A., Silver, Richard T., Siu, Lillian L., Steensma, David P., Stewart, Marc F., Stock, Wendy, Stone, Richard, Storb, Rainer, Strong, Louise C., Tallman, Martin S., Thompson, Michael, Ueno, Naoto T., Van Etten, Richard A., Vose, Julie M., Wiernik, Peter H., Winer, Eric P., Younes, Anas, Zelenetz, Andrew D., and LeMaistre, Charles A.

Published
2015
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39. Wt1 ablation and Igf2 upregulation in mice result in Wilms tumors with elevated ERK1/2 phosphorylation

Author

Hu, Qianghua, Gao, Fei, Tian, Weihua, Ruteshouser, E. Cristy, Wang, Yaqing, Lazar, Alexander, Stewart, John, Strong, Louise C., Behringer, Richard R., and Huff, Vicki

Subjects
Genes -- Physiological aspects -- Research -- Genetic aspects, Insulin-like growth factors -- Genetic aspects -- Research -- Physiological aspects, Protein kinases -- Physiological aspects -- Research -- Genetic aspects, Phosphorylation -- Research -- Genetic aspects -- Physiological aspects, Nephroblastoma -- Development and progression -- Research -- Genetic aspects, Health care industry
Abstract

Wilms tumor (WT) is a genetically heterogeneous childhood kidney tumor. Several genetic alterations have been identified in WT patients, including inactivating mutations in WT1 and loss of heterozygosity or loss of imprinting at 11p15, which results in biallelic expression of IGF2. However, the mechanisms by which one or a combination of genetic alterations results in tumorigenesis has remained challenging to determine, given the lack of a mouse model of WT. Here, we engineered mice to sustain mosaic, somatic ablation of Wt1 and constitutional Igf2 upregulation, mimicking a subset of human tumors. Mice with this combination of genetic alterations developed tumors at an early age. Mechanistically, Wt1 ablation blocked mesenchyme differentiation, and increased Igf2 expression upregulated ERK1/2 phosphorylation. Importantly, a subset of human tumors similarly displayed upregulation of ERK1/2 phosphorylation, which suggests ERK signaling might contribute to WT development. Thus, we have generated a biologically relevant mouse model of WT and defined one combination of driver alterations for WT. This mouse model will provide a powerful tool to study the biology of WT initiation and progression and to investigate therapeutic strategies for cancers with IGF pathway dysregulation., Introduction Wilms tumor (WT) is a childhood kidney tumor that is thought to arise from undifferentiated metanephric mesenchyme. WT is genetically heterogeneous. Mutations that occur in tumors include inactivation of [...]

Published
2011
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43. Abstract PS8-04: Clinical and pathological characteristics and screening outcome for secondary cancers in breast cancer patients with li-fraumeni syndrome attending the MD anderson li-fraumeni education and early detection program clinic

Author

Al-Awadhi, Aydah, primary, Abuhadra, Nour, additional, Liu, Diane D, additional, Barrera, Angelica M Gutierrez, additional, Corredor, Jessica, additional, Strong, Louise C, additional, and Arun, Banu K, additional

Published
2021
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